Pediococcus acidilactici CECT 9879 (pA1c®) and heat inactivated pA1c® (pA1c® HI) ameliorate gestational diabetes mellitus in mice


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Pediococcus acidilactici CECT 9879 (pA1c®) and heat inactivated pA1c® (pA1c® HI) ameliorate gestational diabetes mellitus in mice

Aims: Gestational diabetes mellitus (GDM) is the most common complication of pregnancy and is known to be associated with an increased risk of postpartum metabolic disease. Based on the important role that the intestinal microbiota plays in blood glucose regulation and insulin sensitivity, supplementation of probiotic and postbiotic strains could improve glucose metabolism and tolerance in GDM. Main

methods: 56 4-week-old female C57BL/6J-mice were divided into 4 groups (n = 14 animals/group): control (CNT), high-fat/high-sucrose (HFS), pA1c® alive (pA1c®) and heat-inactivated pA1c® (pA1c®HI). Serum biochemical parameters were analyzed, gene expression analyses were conducted, and fecal microbiota composition was evaluated by shot-gun sequencing. Key findings: pA1c®- and pA1c® HI-supplemented groups presented reduced fasting blood glucose levels and reduced insulin resistance during gestation and exhibited lower visceral adiposity and increased mu scle tissue, together with an improvement in intrahepatic TGs content and ALT levels. Liver gene expression analyses demonstrated that pA1c® and pA1c® HI activities were mediated by modulation of the insulin receptor, but also by an overexpression of beta-oxidation genes, and downregulation of fatty acid biosynthesis genes. Shot-gun metagenomics demonstrated that Pediococcus acidilactici was detected in the feces of all the pA1c® and pA1c® HI-group after the supplementation period (75 % of the microbial profile was Pediococcus acidilactici) in only nine weeks of supplementation, and modulated gut microbiota composition. Significance: These results may be considered as future perspectives for the development of preventive, even therapeutic options for GDM based on hyperglycemia reduction, blood glucose regulation, hepatic steatosis attenuation and insulin resistance alleviation. © 2024

Authors : Yavorov-Dayliev D.; Milagro F.I.; Ayo J.; Oneca M.; Goyache I.; López-Yoldi M.; FitzGerald J.A.; Crispie F.; Cotter P.D.; Aranaz P.

Source : Elsevier Inc.

Article Information

Year 2025
Type Article
DOI 10.1016/j.lfs.2024.123359
ISSN 00243205
Volume 362

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